Professional Documents
Culture Documents
Larissa Morgan
Acknowledgements
The following work represents a lengthy collaborative effort; therefore Id first like to
gratefully acknowledge my supervisors Robert Moran and Dr Craig Hilton for their
contribution, guidance, and patient support in honing this project and bringing it to
completion. Gratitude and recognition are also extended to all my colleagues and
friends, who every week kept me going with feedback, counsel, unending cups of tea,
and much needed comic relief. To my family, thank you does not adequately
express my appreciation for the unwavering support and encouragement you have
given me, which has in no small measure contributed to my achievements. Lastly, to
Tui, who knew exactly what time to sit between me and the monitor thank you for
reminding me when to have a break.
Table of Contents
ACKNOWLEDGEMENTS-------------------------------------------------------------------------------------- 2
TABLE OF CONTENTS----------------------------------------------------------------------------------------- 3
LIST OF FIGURES ----------------------------------------------------------------------------------------------- 5
LIST OF TABLES------------------------------------------------------------------------------------------------- 6
ABBREVIATIONS------------------------------------------------------------------------------------------------ 7
INTRODUCTION ------------------------------------------------------------------------------------------------- 8
BACKGROUND ---------------------------------------------------------------------------------------------------- 8
RESEARCH QUESTION ------------------------------------------------------------------------------------------- 13
SECTION 1: LITERATURE REVIEW---------------------------------------------------------------------- 14
CONCEPTS WITHIN OSTEOPATHY ------------------------------------------------------------------------------ 14
THE AUTONOMIC NERVOUS SYSTEM ------------------------------------------------------------------------- 19
Introduction-------------------------------------------------------------------------------------------------- 19
Influences on autonomic function ------------------------------------------------------------------------- 22
Indicators of autonomic function ------------------------------------------------------------------------- 23
Heart Rate Variability -------------------------------------------------------------------------------------- 24
Influences on heart rate variability ----------------------------------------------------------------------------- 25
Measurement and parameters of heart rate variability -------------------------------------------------------- 28
Limitations of heart rate variability as an indicator of ANS activity ---------------------------------------- 30
PAIN -------------------------------------------------------------------------------------------------------------- 33
Introduction-------------------------------------------------------------------------------------------------- 33
Physiological or sensory dimension of pain ------------------------------------------------------------- 33
Affective or emotional dimension of pain ---------------------------------------------------------------- 34
The autonomic nervous system and pain----------------------------------------------------------------- 35
Delayed onset muscle soreness---------------------------------------------------------------------------- 37
Physiology of delayed onset muscle soreness ----------------------------------------------------------------- 37
Delayed onset muscle soreness as a model of pain ----------------------------------------------------------- 40
Procedure ---------------------------------------------------------------------------------------------------- 64
Intervention ------------------------------------------------------------------------------------------------------- 65
DISCUSSION ------------------------------------------------------------------------------------------------------ 79
Outcomes----------------------------------------------------------------------------------------------------- 79
List of Figures
SECTION 1: LITERATURE REVIEW
FIGURE 1
FIGURE 2
FIGURE 3
SECTION 2: MANUSCRIPT
FIGURE 1
FIGURE 2
FIGURE 3
FIGURE 4
List of Tables
TABLE 1
TABLE 2
Abbreviations
AMI
ANS
DOMS
ECG
Electrocardiogram
HF
High frequency
HPA
Hypothalamic-pituitary-adrenal
HRV
LF
Low frequency
MTJ
Musculotendinous junction
PSD
RSA
SA
Sinoatrial
ULF
Ultra-low frequency
VLF
Introduction
The Review of Literature commences with a background in which historical and
contemporary concepts within the osteopathic profession are outlined, before the main
body of the review which discusses the following topics: concepts within osteopathy;
the autonomic nervous system; and pain.
Background
Spinal manipulation is a form of treatment practised in the manual therapy professions
(e.g. chiropractic, osteopathy, and physiotherapy). Although not formally defined,
many within the manual therapy professions would describe spinal manipulation as
the application of a high-velocity low-amplitude force to the zygopophyseal joint of a
specific spinal segment, which results in cavitation of that joint and is often
accompanied by an audible cracking or popping sound (Gibbons & Tehan, 2006).
Other claimed links between osteopathic manual techniques and reported health benefits include improved biomechanical
efficiency, and improved blood supply and drainage.
Somatic: from the Greek Somatiks, meaning of the body. 1. of or relating to the soma: somatic cells (e.g. cells or tissue that
resides outside the germline). 2. of or relating to an animal body or body wall as distinct from the viscera, limbs, and head. 3. of
or relating to the human body as distinct from the mind: a somatic disease ("The new Collins dictionary and thesaurus," 1988).
More recently, an association between Type II diabetes mellitus and palpable skin
texture change was reported (Licciardone, Fulda, Stoll, Gamber, & Cage, 2007).
Licciardone et al. found the strongest and most consistent of the palpatory findings
assessed (skin changes, trophic changes, tissue changes, tenderness, immobility), to
be tissue changes on the right side of T11-L1 vertebral segments. Yet, many of the
five palpatory elements assessed showed little difference between right and left, even
though much of the pancreas is located left of the bodys midline. Furthermore, the
most consistent skin texture changes were found at the level of T11-L1, a segmental
level beyond the autonomic supply of the pancreas presented in many undergraduate
physiology texts (T6-T10). Licciardone et al. speculated that reflex viscerosomatic
changes directly related to the progression of type Type 2 diabetes mellitus might be
responsible for the results, but could not eliminate the possibility of a spurious
association or chance observation. Based on sparse and inconclusive literature, the
link between visceral disease and musculoskeletal changes is not a clear and causal
one, and could be considered associative at best. Moreover, if frank pathology does
not manifest in consistent or clearly observable musculoskeletal changes, the
osteopathic concept that non-pathological disturbance may result in similar change is
less plausible.
branches of nerves other than those that innervate the actual source of pain, or in
clinical terms as pain perceived as occurring in a region of the body topographically
distinct from the region in which the actual source of pain is located (Merskey &
Bogduk, 1994, p. 12).
Referred pain is not an autonomic reflex although may be associated with such
reflexes. As a phenomenon, referred pain has long been recognised, with descriptions
dating to the late 19th century (Ross, 1888, Ruch, 1961, & Sturge, 1883, as cited in
Arendt-Nielsen & Svensson, 2001). Several theoretical models have been developed
to explain the occurrence of referred pain, with the current and most accepted model
being the convergence-projection theory (Arendt-Nielsen & Svensson, 2001). This
theory is broadly similar to the osteopathic concept regarding autonomic reflexes in
that the proposed mechanism is one of convergence. Although not wholly
understood, referred pain is thought to occur by the following means: pain signals
from injured tissue and normal sensory signals from other tissues converge within the
dorsal horn of common spinal segments, however, in the barrage of information, the
spinal cord cannot clearly distinguish the origin of the pain signal, and so a noninjured area is perceived to be painful (Arendt-Nielsen, Laursen, & Drewes, 2000;
Arendt-Nielsen & Svensson, 2001; Giamberardino, Affaitati, Lerza, & Vecchiet,
2000). Due to the clinical significance of referred pain (e.g. myocardial ischemia and
pain in the left arm), this phenomenon is the most widely acknowledged and studied
interaction between somatic and visceral structures.
In contrast to the referred pain phenomenon, the concept that somatic and visceral
disturbance can influence other structures though the ANS has limited scientific
support. With few human studies available, osteopathic literature has often relied on
evidence from experiments on laboratory animals. Conclusions from these
experiments, which are cited frequently and with little critique in osteopathic
literature, are that stimulation of visceral and somatic nerves produce responses in
cardiac ANS activity (Terui & Koizumi, 1984), and that noxious or painful
musculoskeletal stimuli clearly and consistently modulate ANS activity and
sometimes visceral function (Adachi, Meguro, Sato, & Sato, 1990; Kaufman, Sato,
Sato, & Sugimoto, 1977; Sato, Sato, & Schmidt, 1997; Sato & Schmidt, 1987). Many
of the same investigators have also found that innocuous mechanical stimuli affect the
11
ANS, albeit in a milder and less consistent manner than noxious stimuli (Sato et al.,
1997; Sato & Swenson, 1984). Yet, within osteopathic literature, the findings
regarding innocuous stimulation on the ANS are cited infrequently, potentially
exposing a bias towards citing scientific data that supports osteopathic concepts.
More recently, osteopathy and other manual therapies have begun to formally
investigate whether manual therapeutic techniques influence the ANS. Evidence has
emerged showing that spinal manipulation and innocuous non-spinal stimulation
affect autonomic activity (Budgell & Hirano, 2001; Budgell & Polus, 2006; Cooper,
2006; Driscoll & Hall, 2000; Eingorn & Muhs, 1999; Knutson, 2001; McGuiness,
Vicenzino, & Wright, 1997; Zhang, Dean, Nosco, Strathopulos, & Floros, 2006);
however, clinical outcomes have not been included in these studies. To date, studies
have focused on the cause-effect relationship between manual therapy techniques and
the ANS without regard to magnitude of effect, and whether such effect is clinically
favourable or unfavourable. Furthermore, the investigations have not ascertained
whether techniques that are purported to modulate the ANS are a necessary, or
clinically relevant, part of care. The issue of clinical relevance is further weakened by
insufficient critical review of the findings: any ANS effects observed in these
investigations could be epiphenomena and not part of the causal chain purported to
exist between musculoskeletal disturbance and effects elsewhere in the body.
On balance, the osteopathic concept that musculoskeletal disturbance can perturb the
ANS is lacking support. The poorly elucidated mechanisms, inadequate appraisal of
clinical relevance, and limited scope of research places the concept in a contentious
light despite associations suggested by current literature (Licciardone et al., 2007).
It comes as no surprise then, as Stone (1999, p. 75) indicates in a contemporary
osteopathic text, that the concept of musculoskeletal irritation causing visceral
disturbance is not a recognised clinical entity. Yet, within osteopathic textbooks and
in oral history imparted in undergraduate training, the concept remains fundamental.
The osteopathic profession maintains the long held position that manual therapeutic
techniques favourably influence the ANS and are an appropriate part of care.
Dogma, coupled with limited and often inconclusive evidence, has done little to avert
any controversy surrounding the concept that somatic or visceral disturbance affects
12
Research question
The aim of this pilot study was to explore whether delayed-onset muscle soreness
(DOMS), as a model of pain and mild musculoskeletal injury, would affect the ANS
as measured by heart rate variability (HRV). The rationale for employing DOMS was
that it is simple to induce, non-invasive, and would simulate a soft tissue injury
without involving gross trauma or heterogeneity of damage.3 Heart rate variability
has been employed in a variety of fields to evaluate changes to the ANS, and although
not a direct measure of mean autonomic tone, HRV was considered a well supported
measure for this project.
Heterogeneity is used here to denote damage involving tissue types other than myofascia, such as bone, ligament, cartilage,
nerves, and blood vessels.
13
Within osteopathy, the approach to treatment is guided by several concepts, such as:
(DiGiovanna et al., 2005, pp. 10-15; Kuchera & Kuchera, 1993, p. 2; Nelson,
2007b, pp. 6-11).
Although these concepts are not unique to osteopathy, they help form the basis of the
osteopathic perspective on health and disease.
Health, illness, and disease are concepts that differ between cultures and historically
have been rich with theory and debate. Osteopathic texts regard health and disease as
an interplay and balance between the emotional, chemical, and physical environments
(DiGiovanna et al., 2005, pp. 10-15; Kuchera & Kuchera, 1993, pp. 7-12; Stone,
1999, pp. 15-27). The notion within osteopathy is that failure to adapt, or exposure to
overwhelming external factors, can upset the balance between these environments and
can prevail over the bodys capacity for self-maintenance (DiGiovanna et al., 2005;
Stone, 1999). As a form of manual medicine, osteopathy emphasises the role the
neuromusculoskeletal system plays in the manifestation of health and disease
(DiGiovanna et al., 2005).
The concepts of normal function and dysfunction are commonly used within the
osteopathic profession. Yet, these terms are hampered in a similar manner as that of
health and disease. Stone (1999, pp. 28-56) has reasoned that disease may be
14
Theorists within osteopathy surmise that the anatomical arrangement of the ANS,
particularly the sympathetic division, makes the ANS accessible to osteopathic
manual treatment. For example, within osteopathy, the perceived accessibility of
sympathetic division permits the ANS to be influenced, albeit indirectly, with
techniques such as spinal manipulation. Although spinal manipulation has, in recent
times, been shown to have an effect on the ANS the mechanisms remain unclear
(Pickar, 2002; Willard, 2007; Wright, 1995). Nonetheless, many osteopaths maintain
the view that balance and integration of ANS subdivisions has a significant role in
health and disease, (DiGiovanna et al., 2005; Stone, 1999). As such, disturbance of a
15
Acute somatic dysfunction: Immediate or short-term impairment or altered function of related components of the somatic
(body-framework) system; characterised in early stages by vasodilation, oedema, tenderness, pain and tissue contraction
Chronic somatic dysfunction: impairment or altered function of related components of the somatic (body-framework) system,
characterised by tenderness, itching, fibrosis, paraesthesias, tissue contraction
Primary somatic dysfunction: 1) The somatic dysfunction that maintains a total pattern of dysfunction. 2) The initial or first
somatic dysfunction to appear temporally.
Secondary somatic dysfunction: somatic dysfunction arising either from mechanical or neurophysiologic response subsequent
to or as a consequence of other aetiologies (Glossary of Osteopathic Terminology, 2004)
16
such effects may be attributed remain inconclusive. The diverging results seen in the
literature has prompted Pickar (2002) to suggest that more than one mechanism
likely explains the effects of spinal manipulation, and theories continue to abound
regarding what therapeutic processes or physiological mechanisms are involved
(Wright, 1995). Nonetheless, the effect of spinal manipulation on the ANS comprises
only one aspect within the concept that musculoskeletal or visceral disturbance can
perturb the ANS. Other aspects, such as whether ANS perturbation does occur and
can be objectively measured, or indeed is clinically relevant, have not been adequately
investigated.
18
Central Nervous
System
Peripheral
Nervous System
Sensory
Motor
Autonomic
Nervous System
(Involuntary)
Sympathetic
division
Figure 1
Somatic Nervous
System
(Voluntary)
Parasympathetic
division
Texts describe both divisions of the ANS as displaying segmental organisation in the
innervation of the body (Figure 2). In the sympathetic nervous system, fibres exit the
spinal cord between the first thoracic and second lumbar vertebra. The fibres then
pass to the sympathetic trunk ganglia flanking these vertebrae and follow one of three
courses: synapse immediately at the same level; travel within the sympathetic trunk to
synapse at a higher or lower level; or pass through the sympathetic trunk to synapse
with prevertebral ganglia. In contrast, the parasympathetic nervous system has a more
restricted distribution. Fibres originate from cell bodies within the brainstem and the
second to fourth sacral segments of the spinal cord to synapse close to the target
organ. The vagus nerve in particular is central to regulation of visceral organs as
numerous vagal branches provide much of the parasympathetic innervation of
thoracic and abdominal organs.
Sympathetic
Parasympathetic
CN III
Eye
CN VII
CN IX
Eye
CN X
Heart
Lungs
T1
Parotid gland
Heart
Lungs
Upper gastrointestinal tract
Adrenal medulla
S2 S4
Figure 2
20
To maintain homeostasis, the ANS detects and responds to a variety of stimuli in the
internal and external environment. This activity results in continual moment-tomoment responses and is commonly thought to be regulated by higher centre control
and peripheral reflex arcs. Yet, as Janig and McLachlan (1992; 1999) observe, the
diversity of the ANS is not limited to a simple neuroendocrine role, as discrete
functional pathways and differentiation of reflex patterns have been identified at
molecular, cellular, and integrative levels. The complex neuroendocrine role of the
ANS is reflected in specialisation of the vagus nerve of the parasympathetic system.
Berthoud and Neuhuber (2000) describe the vagus as having a peripheral and central
interface: mechanical, chemical, and temperature receptors are found in and around
organs, and the vagus also projects to the brainstem and forebrain. Berthoud and
Neuhuber go on to discuss evidence regarding a vagal role in pain perception, in both
a sensory and affective capacity, and that the anatomical connections of the vagus
imply a potential for vagal signals to affect the entire organism.
Parasympathetic activity to the heart, mediated by the vagus nerve, produces states of
relaxation and calm. Increased vagal activity to the sinoatrial node reduces heart rate
and blood pressure, increases the beat-to-beat variability of the heart, and reduces
force of contraction. Vagal governance of respiration also modulates cardiovascular
function via respiratory depth and frequency (Task Force of the European Society of
Cardiology and the North American Society of Pacing and Electrophysiology, 1996).
Vagal activity therefore regulates cardiovascular function through a direct contact
with the SA node, and modulates heart rate and blood pressure through respiration
(Stauss, 2003).
22
Numerous intrinsic factors, such as circadian rhythms and metabolic products, are
recognised to have a widespread influence on the ANS. Extensive and often
detrimental influences on the ANS are associated with many pathologies, such as
endocrine, renal, and neurological disorders (Mathias & Bannister, 1999).
Widespread effects on the ANS are also linked with aging (Docherty, 2002) and in
consumption of chemical agents such as pharmaceuticals, alcohol, and recreational
drugs (Brooks et al., 1979).
Although much knowledge regarding the ANS has unfolded in the last century, many
questions still remain. Berthoud and Neuhuber (2000) comment that the mechanisms
behind central regulation of ANS outflow patterns requires further exploration.
Within the manual therapy professions, questions have predominately focused on
whether autonomic activity is influenced by the mechanical stimulation provided by
manual therapy techniques.
The status of the ANS can be directly assessed with scintigraphic and cardiovascular
reflex tests. As these types of tests are invasive and not widely available, heart rate
variability (HRV) has emerged as a simple non-invasive technique which evaluates
23
sympathetic and parasympathetic activity at the sinoatrial level (Sztajzel, 2004; Task
Force, 1996).
Variation in the R-R interval represents the subtle regulation of the dynamic
cardiovascular control mechanisms by the ANS. The sympathetic and
parasympathetic activity directed to the sinoatrial node is mostly synchronous with
each cardiac cycle, but can be modulated by central and peripheral oscillators such as
the respiratory centre in the brainstem, or arterial baroreceptors (Task Force, 1996).
The modulations cause a rhythmic fluctuation in sympathetic and parasympathetic
discharge which manifests as short and long-term oscillations in the cardiac
contraction period. Analysis of these oscillations may permit inferences to be made
on the state and function of sympathetic and parasympathetic activity, the central
oscillators, humoral factors, and the sinoatrial node itself (Task Force, 1996).
Figure 3
24
The clinical utility of HRV is reflected in numerous published works on HRV in the
context of cardiovascular physiology and medicine (Berntson et al., 1997). Reduced
HRV is strongly associated with adverse outcomes (Dekker et al., 2000; Dekker et al.,
1997; Liao et al., 1997; Tsuji et al., 1996), and HRV data has demonstrated that
sympathetic activity is elevated in heart failure and coronary artery disease, and plays
a role in hypertension (Eisenhofer et al., 1996; Huikuri et al., 1996; McCance,
Thompson, & Forfar, 1993). Reduced HRV has been shown to be of prognostic
relevance in progressive heart failure and is associated with increased mortality after
acute myocardial infarction (La Rovere, Bigger, Marcus, Mortara, & Schwartz, 1998;
La Rovere et al., 2003; Ponikowski et al., 1997). Consequently, the most common
clinical application of HRV is predicting risk of death in patients with cardiac disease
(Bigger et al., 1995).
25
Chaos theory has been utilised to understand a variety of different processes. These
range from fluid turbulence (Kaplan & Yorke, 1979) and weather (Lorenz, 1963;
Pool, 1989b), to biological processes such as epidemics (Olsen & Degn, 1985; Pool,
1989a), biochemical reactions (Decroly & Goldbeter, 1982, 1985), and cardiac
behaviour (Goldberger, Findley, Blackburn, & Mandell, 1984; Goldberger, Shabetai,
Bhargava, West, & Mandell, 1984). To illustrate the characteristics of chaotic
behaviour, that is, periodic from one viewpoint yet random from another, Denton,
Diamond, Helfant, Kahn, & Karaqueuzian (1990) offer the following examples: the
average behaviour of a container of gas molecules can be predicted, however the
individual behaviour of a single molecule cannot; likewise, the average heart rate of a
patient can be predicted, however the individual pattern of R-R intervals cannot.
The HRV data from a patient with heart failure shows reduced or restricted variability
of the R-R intervals (Goldberger, 1997; Goldberger, Findley, Blackburn, & Mandell,
1984). Restricted variability is one that is more uniform and periodic, and shows
predictable oscillations in the heart rate. In contrast, the HRV from a healthy heart
demonstrates a variability which is more complex, less uniform, and more irregular.
The complexity of the variation seen in healthy subjects has lead to the suggestion that
a healthy cardiovascular system is one that can generate chaos (Denton et al., 1990).
Research by Goldberger, who draws heavily on chaos theory, has in the past three
decades provided insight into cardiovascular physiology and disease. Goldberger
(1996) has remarked that a healthy heart beat is chaotic and states that This kind of
complex variability, rather than a regular homeostatic steady state, appears to define
the free-running function of many biological systems. A loss of complex variability
in the cardiovascular system is proposed to be a common feature of cardiovascular
disease. Such loss of complexity, that is, a more predictable and less chaotic state,
means less adaptive capacity in a dynamic environment (Goldberger, 1997;
Kobayashi & Musha, 1982; Lipsitz & Goldberger, 1992; Peng et al., 1993).
The complexity of the cardiovascular system is reflected in the linear and non-linear
influences in its environment. Many of the same extrinsic and intrinsic factors that
influence the ANS also influence HRV. Extrinsic factors include posture (Montano et
al., 1994), exercise (Pober, Braun, & Freedson, 2004; Uusitalo, Laitinen, Vaisanen,
26
Lansimies, & Rauramaa, 2004), mental stress and physical stress (Delaney & Brodie,
2000; Terkelsen, Andersen, Molgaard, Hansen, & Jensen, 2004). Intrinsic factors
include respiratory sinus arrhythmia (Yasuma & Hayano, 2004), sleep processes
(Viola et al., 2002), temperature and neuroendocrine regulation (Task Force, 1996),
and circadian rhythms (Bonnemeier et al., 2003; Molgaard, Sorensen, & Bjerregaard,
1991; Scheer, Van Doornen, & Buijs, 2004).
Chemical agents that modulate the ANS also influence HRV, including certain
medicines, caffeine, tobacco, and alcohol (Kupari, Virolainen, Koskinen, & Tikkanen,
1993; Task Force, 1996). Smoking (Hayano et al., 1990) and alcohol consumption
(Kupari & Koskinen, 1993) are related to impaired autonomic function, which can
affect HRV. However, lifestyle factors such as these also show gender (JensenUrstad, Jensen-Urstad, Ericson, & Johansson, 1998) and personality (Kamada,
Miyake, Kumashiro, Monou, & Inoue, 1992) variation.
the HPA axis has been associated with alcoholism (Adinoff, Iranmanesh, Veldhuis, &
Fisher, 1998; Thayer, Hall, Sollers, & Fischer, 2006), and impairment of the HPA
axis in heavy drinkers appears to lower HRV (Thayer et al., 2006). Dysregulation of
the HPA axis is also linked with epilepsy (Zobel et al., 2004) and disorders such as
depression, schizophrenia, and anxiety (Drevets, 1999; Thayer & Friedman, 2002).
An impaired HPA axis from affective disorders such as these can also alter cardiac
autonomic tone (Bar et al., 2004; Cohen & Benjamin, 2006; Udupa et al., 2007).
The popularity of PSD stems from the computational ease provided by the nonparametric Fast Fourier Transform. Auto-regressive parametric methods are also used
for PSD but tend to be more complex and the suitability of the chosen model requires
28
verification (Sztajzel, 2004; Zhong et al., 2006). The power spectrum of HRV is
routinely classified into four frequency bands (Task Force, 1996):
1. ultra-low frequency (ULF) (0.0033-0.05 Hz)
2. very low frequency (VLF) (0.003-0.04 Hz)
3. low frequency (LF) (0.04-0.15 Hz)
4. high frequency (HF) (0.15-0.4 Hz).
The boundaries between frequencies are not fixed and may vary with changes to the
autonomic control of the heart. Therefore the ranges defined represent a pragmatic
delineation rather than a functional basis (Sztajzel, 2004; Task Force, 1996).
The remaining frequency bands can be extracted with shorter-term HRV recordings.
Thermoregulation has been suggested as the primary influence on VLF, although
diverse stimuli and conditions have also been found to contribute. These include
haemorrhage, acidosis, alkalosis, high altitude, posture, congestive heart failure,
breathing patterns, and spinal reflexes (Stauss, 2003). While the determinants of the
VLF and ULF bands is not as well known as the other bands, these components are
thought to account for as much as 95% of 24-hour total power (Pikkujamsa, 1999).
The low frequency band has previously been proposed as an index of pure
sympathetic activity. Recent studies suggest that LF is mediated by both sympathetic
and parasympathetic traffic (Stauss, 2003; Sztajzel, 2004; Task Force, 1996; Zhong et
al., 2006). Baroreceptor activity is thought by some to be the predominant influence
on LF (Sleight et al., 1995), although some human (Cooley et al., 1998) and animal
data (Montano et al., 1996) suggests a medullary origin. Since LF is not specific for
29
30
al., 2005; Malpas, 2002; Radespiel-Troger, Rauh, Mahlke, Gottschalk, & MuckWeymann, 2003).
The Task Force (1996) points out that measurement, analysis, and interpretation of
HRV has clear pitfalls and caveats that need to be considered by researchers and
clinicians utilising these methods. Research literature is equivocal regarding the most
accurate HRV parameter for clinical use, underpinned by the need for clear
elucidation of the putative link between reduced HRV and mortality (Sztajzel, 2004).
Large intra-individual variation in autonomic function, such as age, gender,
pharmacological agents, psychology, and concomitant disease are also recognised as
factors that prevent prescription of a standardised method of HRV assessment (AbdelRahman, Merrill, & Wooles, 1994; Huikuri et al., 1990; Kupari, Virolainen,
Koskinen, & Tikkanen, 1993).
A further limitation is that stability over time of short-term HRV recordings has
shown variable reliability (Kleiger et al., 1991; Sandercock, Bromley, & Brodie,
2005; Tarkiainen et al., 2005). Coefficients of variation have ranged from <1% to
>100%, and with the absence of Task Force recommendations, targets for acceptable
levels of reliability (4-30%) have been adopted by various investigators on an
apparently arbitrary basis. Despite the wide range of reliability described in the
literature, satisfactory intra-individual reproducibility of 24-hour recordings has been
demonstrated in both healthy populations and those with known heart disease
(Huikuri et al., 1990; Kleiger et al., 1991). With the issues surrounding the stability
of HRV data, the Task Force has recommended that, for clinical purposes, HRV
should only be used to warn of early diabetic neuropathy and predict risk of death
after acute myocardial infarction (AMI).
Heart rate variability has also shown modest or limited sensitivity, specificity, and
positive predictive accuracy in cardiovascular disease. The Task Force has advised
that predictive relationships based on HRV can be degraded by cardiac or neural
abnormalities, autonomic interactions, and respiratory parameter variability.
Moreover, artifact and ectopic beats during HRV recording can considerably interfere
with estimates and may invalidate the measurement or lead to over-editing of raw data
(Pikkujamsa, 1999). The differences in diagnostic odds of HRV between recent and
31
32
Pain
Introduction
Pain has been defined as An unpleasant sensory and emotional experience associated
with actual or potential tissue damage, or described in terms of such damage
(Merskey & Bogduk, 1994, p.210). One component of pain5 is nocioception, which
describes the physiological signal that occurs from stimulation of free nerve endings
(nocioceptors) by stimuli considered capable of causing tissue damage (Siddall &
Cousins, 1997). But, as Melzack and Wall (1965) state, the experience of pain and
nocioception are not one and the same. Pain is considered to involve higher centres
associated with cognition, emotion, and sensation, and that actual or potential tissue
damage stimulates feedback circuits that result in behavioural and autonomic
responses. Although clinical pain management can be hobbled by the mind-body
dichotomy, greater knowledge of the affective-emotional dimension of pain has lead
to better understanding of chronic pain, coping strategies, and effective interventions.
Components of pain: nocioception (stimulation of free nerve endings from noxious or tissue damaging stimulus), pain
perception (i.e. cognitive or sensory awareness of pain), pain behaviours such as wincing that are observable behavioural
responses, and personal suffering which is the emotional reaction to pain (Loeser & Melzack, 1999; Merskey & Bogduk, 1994).
33
prolonged, gene induction in the dorsal root ganglia and the dorsal horn of the spinal
cord occurs. This may result in central sensitisation, a term that describes longer-term
alteration in sensory nerve responsiveness, the development of cellular memory for
pain, and the development of connections with nerves that conduct mechanical stimuli
(Siddall & Cousins, 1997). Central sensitisation causes heightened sensitivity of
sensory neurons in a wider area by contributing to the phenomena of allodynia6 and
secondary hyperalgesia7 (Butler, 2000; Siddall & Cousins, 1997).
Attentional bias is a term used in psychology and pain literature which refers to the
tendency toward a particular cognitive strategy to cope with pain. Attentional biases
include ignoring, distraction, catastrophising, positive appraisal, reinterpretation, and
praying (Boothby, Thorn, Stroud, & Jensen, 1999, pp. 343-359.; Keogh et al., 2000).
Research demonstrates that attentional biases such as distraction, avoidance, or
focused attention, affect the speed and accuracy of noxious stimulus detection and
therefore the perception of pain (Miron, Duncan, & Bushnell, 1989).
Allodynia: Pain due to a stimulus which does not normally provoke pain (Merskey & Bogduk, 1994, p. 210)
Hyperalgesia: An increased response to a stimulus which is normally painful (Merskey & Bogduk, 1994, p. 211). Secondary
hyperalgesia is heightened responsiveness of the surrounding uninjured tissue (Butler, 2000).
34
2001; Vlaeyen & Crombez, 1999). In chronic musculoskeletal pain this postulate is
known as the fear-avoidance model (Asmundson & Hadjistavropoulos, 2007) or
fear of (re)injury model (Vlaeyen & Linton, 2000).
Threat value is an important factor in pain as perceived threat demands attention and
higher centre resources (Crombez, Baeyens, Vansteenwegen, & Eelen, 1997;
Moseley, Brhyn, Ilowiecki, Solstad, & Hodges, 2003). Threat value is highly
subjective, and intrinsically linked to fear of pain, attentional bias, control, and
context (Moseley et al., 2003; Munafo & Stevenson, 2003; Vlaeyen & Linton, 2000).
The situational context and meaning ascribed to pain has been shown to have a
particularly significant influence on threat value (Bayer, Baer, & Early, 1991; Smith,
Gracely, & Safer, 1998). To illustrate, Moseley (2003) uses the example that a
professional violinist with a minor finger injury will experience greater pain as the
damage is overlaid with a threat to livelihood and identity. In a person whose
livelihood is not dependant on a high level of finger function, the same minor finger
injury may be experienced as less threatening, and therefore less painful.
A further element associated with threat is that of predictability. Rhudy & Meagher
(2000) have proposed that the possibility of shock induces anxiety, whereas
predictable yet unavoidable shock induces fear. These two emotions have differing
effects on pain. Fear appears to evoke a phenomenon known as stress-induced
analgesia where pain is attenuated by release of endogenous opioids (Rhudy &
Meagher, 2000). Anxiety, a future-oriented emotion, results in apprehensive
anticipation of potential threat which leads to increased environmental and somatic
(body) scanning. The anxiety state can therefore facilitate increased sensory
receptivity and enhance pain (Rhudy & Meagher, 2000). Furthermore, the
anticipation of threat in the absence of actual exposure is enough to potentiate startle
reflexes and autonomic responses (Bradley et al., 2008).
35
recognised to include heart rate changes, sweating, and raised serum and salivary
cortisol levels. When confronted with actual or potential damage, the ANS activates
higher centres to co-ordinate strategies and patterns of defence behaviour (Butler,
2000). In a review on pain and autonomic reactions, Benarroch (2001) outlines that
these higher centre mechanisms are invoked via direct projections from the dorsal
horn of the spinal cord to the brainstem, and provide the basis of autonomic,
endocrine, and behavioural responses. The responses include anti-nocioceptive
mechanisms such as cardio-respiratory and renal system changes, analgesia which is
independent of endogenous opioids, and motivational modulation of pain (Benarroch,
2001).
36
Clinical studies have found that the most effective way to induce DOMS is with
eccentric exercise. During eccentric exercise the contracting muscle is forcibly
lengthened, placing high tension on muscle fibres and connective tissue (Proske &
Morgan, 2001). The disruption to skeletal muscle from unaccustomed exercise is not
considered permanent and is not associated with disruption to articular, vascular,
neurological, or osseous structures (Friden, 2002; Proske & Morgan, 2001).
Described in temporal terms, unaccustomed or strenuous exercise causes microdamage to muscle fibres but no soreness immediately after exercise. The mechanical
disruption disturbs the chemical milieu of muscle which is proposed to trigger a
subsequent inflammatory response. The inflammatory response develops over several
hours, and inflammatory mediators such as bradykinin are believed to stimulate free
nerve endings and sensitise them so as to respond to normal innocuous stimuli (also
known as peripheral sensitisation) (Mense & Meyer, 1988; Proske & Morgan, 2001).
37
There is some debate within the literature regarding the proposed mechanisms
involved in DOMS. Inflammation subsequent to damage is not always confirmed
(Malm et al., 2000; Nosaka, Newton, & Sacco, 2002; Vincent & Vincent, 1997) and
the muscle damage theory has too been challenged (Friden & Lieber, 2001; Newham,
1988). Blaise et al. (1999) contend that while some inflammatory mediators are
known to stimulate nocioceptors, the involvement of many of these substances in
DOMS remains largely hypothetical.
Conjecture also surrounds the involvement of connective tissue in the DOMS process.
Graven-Nielsen, Gibson, and Arendt-Nielsen (2006) have recently implicated the role
of fascial tissue in DOMS. Based on subjective reports by research participants, other
investigators have proposed that mechanical damage to the musculotendinous
junction (MTJ) stimulates the dense free nerve endings found at the MTJ and signals
nocioception (Cleak & Eston, 1992). Yet, the nociceptive characteristics of tendon
are not clear (Gibson, Arendt-Nielsen, & Graven-Nielsen, 2006) and other studies
indicate this effect may depend on the amount of damage at the MTJ (Bajaj, GravenNielsen, & Arendt-Nielsen, 2001; Eston, Critchley, & Baltzopoulos, 1994), and how
large the muscle attachment area is (Bajaj et al., 2001; Brand, Beach, & Thompson,
1981).
Some reports propose that central mechanisms may be important in pain associated
with DOMS. Gibson et al. (2006) suggest that central sensitisation may be involved
after finding greater referred pain frequency and enlarged pain areas during DOMS
38
Despite the exact mechanisms being unclear, there is general agreement that DOMS
appears to be beneficial in terms of the objective properties of muscle. Yu et al.
(2004) propose that remodelling as opposed to damage is the mechanism at work,
supported by the so-called repeated-bout effect. The repeated-bout effect occurs
when subsequent bouts of eccentric exercise, from 1-10 weeks after the initial bout,
produce much less muscle damage implying an adaptive and protective function
(Ebbeling & Clarkson, 1989; Golden & Dudley, 1992; Nosaka, Clarkson, McGuiggin,
& Byrne, 1991; Paddon-Jones, Muthalib, & Jenkins, 2000). Even second bouts
performed during the early recovery period (1-5 days) of an initial bout have not
exacerbated muscle damage or retarded the recovery process (Ebbeling & Clarkson,
1989; Paddon-Jones et al., 2000), with some studies showing this effect regardless of
the intensity and volume of eccentric action performed in the second bout (Chen &
Nosaka, 2006). Light eccentric exercise, which does not significantly change markers
39
of muscle damage, is also believed to confer a protective effect (Lavender & Nosaka,
2008).
As the aim of this project was to explore mild to moderate musculoskeletal injury on
the ANS, DOMS was selected as a model of tissue injury that could be induced under
controlled conditions. Compared to naturally occurring injuries, using a DOMS-
40
model would partially control for variability in severity and damage to tissues other
than myofascia. The temporal nature of DOMS was considered useful to compare
subjective appraisal of pain with the sequence of events thought to occur in DOMS.
Since DOMS is not associated with chronicity, and believed to have an adaptive role,
DOMS may be considered an ethically appropriate model of pain to use in
experimental research.
41
The mechanisms underlying spinal manipulation have not been fully elucidated.
There is also limited evidence regarding the other links in the purported causal chain
between visceral and musculoskeletal disturbance and the ANS. Nonetheless, the
primary focus of previous investigations has been the cause-effect relationship
between spinal manipulation and the ANS. Osteopathy has a number of areas to
evaluate, for example: whether mild to moderate musculoskeletal disturbance affects
the ANS; what magnitude of effect spinal manipulation has on the ANS; whether the
direction of such an effect is favourable or not; and the clinical significance of the
techniques. The objective of the investigation documented in Section 2 of this
dissertation was to determine whether a mild musculoskeletal disturbance, such as
that evident in DOMS, has the capability to influence the ANS as measured by heart
rate variability.
42
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54
55
Section 2: Manuscript
Note
This manuscript has been prepared in accordance with the Guide for Authors for the International
Journal of Osteopathic Medicine (See Appendix E).
56
57
Larissa Morgan
School of Health Science
Unitec New Zealand
Private Bag 92025, Auckland
New Zealand
58
Abstract
Background: A central concept within osteopathy is that disturbance of
musculoskeletal or visceral structures can perturb the autonomic nervous system
(ANS). Such perturbation is postulated to generate reflexes that can affect other
structures with the same autonomic innervation. Within osteopathy, the effects of this
purported process are considered amenable to manual therapy techniques, such as
spinal manipulation. However, scientific research investigating this process is limited
and often inconclusive, and despite evidence demonstrating that spinal manipulation
affects the ANS, the clinical relevance of such an effect has had limited discussion.
Objective: The objective of this study was to examine the effect of a mild to
moderate musculoskeletal disturbance, such as delayed onset muscle soreness
(DOMS), on the ANS as measured by heart rate variability (HRV), in healthy young
males.
Methods: A time series single-subject design was conducted on six subjects (age
range 23 to 36 years). Heart rate was recorded daily for 15 minutes over five
consecutive days to establish baseline (Phase A) and then daily for nine consecutive
days after an exercise protocol to induce DOMS (Phase B). Pain intensity scores
were recorded twice daily throughout Phase B. Frequency spectra for HRV data was
extracted and five minutes of normalised R-R intervals were plotted with pain
intensity data against time. Visual analysis of changes to level, trend, and stability of
HRV and pain intensity data was then performed.
Results: Within the confines of this study, the results indicated that changes to HRV
did not occur as a result of pain associated with DOMS. Although slight differences
in the stability of HRV data and slope of trend line occurred in some subjects, no
consistent pattern emerged that was attributable to DOMS.
Conclusion: Delayed onset muscle soreness was not clearly associated with changes
to the autonomic output to the heart, as measured by HRV, in healthy males.
Key terms: Autonomic nervous system; Heart rate variability; Delayed onset muscle
soreness; time-series design.
59
Introduction
A central concept within osteopathic texts is that disturbance of musculoskeletal
structures can perturb the autonomic nervous system (ANS). Perturbation of the ANS
is believed to potentially influence the function of viscera or other musculoskeletal
structures supplied by common autonomic segments.1, 2 The osteopathic concept that
disturbance to visceral and musculoskeletal structures can have effects elsewhere in
the body via the ANS, is commonly described in historical and anecdotal reports but
has not been adequately investigated. This concept also provides part of the rationale
for the osteopathic treatment approach and the use of spinal manipulation techniques.
Although research indicates that noxious and long-term musculoskeletal stimuli can
produce changes in the ANS,3-5 the effects from mild to moderate musculoskeletal
disturbance are less apparent.6-10
Osteopathic literature has begun to gather evidence on one aspect of the concept that
musculoskeletal or visceral disturbance can perturb the ANS: namely, whether
manual therapy techniques, such as spinal manipulation, influence autonomic activity.
Recent evidence has demonstrated that spinal manipulation appears to exert an effect
on the ANS,9, 11, 12 however, these studies do not indicate the magnitude of effect nor
whether the effect on the ANS is favourable or unfavourable. Furthermore, it is not
clear how clinically beneficial techniques that putatively influence the ANS are, nor
how necessary such techniques are to patient care.
Recently, a case series study by Grimm et al. investigated soft tissue injury and ANS
indices.7 Although Grimm reported alterations in cardiac and peripheral autonomic
activity amongst injured subjects, there is scant literature investigating a possible
relationship between soft tissue injury and ANS perturbation. With few studies, and
no clear physiological mechanisms, evidence to support or refute the osteopathic
concept that musculoskeletal disturbance can perturb the ANS is lacking.
Furthermore, it is unclear whether it necessarily follows that such ANS perturbation
will have an unfavourable effect. If osteopathic techniques can modulate ANS
activity, do they evoke an ANS response beyond any localised or short-term general
effect, to ameliorate the so-claimed effects further afield? Establishing the nature and
60
significance of any purported links is important to not only evaluate tenets within
osteopathy, but may be of clinical relevance to those with acute injury or those in
chronic pain states.
61
Methods
Design
A time-series A-B experimental design was used for this preliminary study. Timeseries or single-subject designs are a useful low-cost approach to provide preliminary
information about possible causal relationships.13-15 Such designs are logistically
simple and may provide avenues for further investigation with more robust group
designs such as randomised, controlled, experimental studies.
Subjects
Subjects were recruited via word of mouth and poster advertising at Unitec New
Zealand. All subjects satisfied exclusion and inclusion criteria. Exclusion criteria
were: disorders of the immune, endocrine, and musculoskeletal systems; recent or
unresolved trauma; psychological disorders; and medication known to influence the
ANS or cardiovascular system. Exclusion criteria also included participation in highintensity or frequent cardiovascular or resistance exercise (five or more days per
week), such as high-intensity cycling, running, or weight training. Subjects were
required to be non-smokers, with a body mass index (BMI) between 18.5 and 30, and
not experiencing pain or discomfort at the time of recruitment. The Unitec Research
Ethics Committee approved the study and written informed consent was obtained
from all subjects [see Appendix A].
62
Independent variable
The intended tissues in which DOMS was to be induced were the elbow flexor, and
possibly forearm flexor, muscles of the non-dominant arm. The manner in which
DOMS was induced was consistent with previous studies on DOMS,16-18 utilising
eccentric contraction of the elbow and forearm flexor muscles to produce controlled
elbow extension to the end of range. The maximum weight able to be performed for a
single repetition of elbow flexion, or one repetition maximum (1RM), was
ascertained, and isokinetic eccentric contraction of the elbow and forearm flexors was
performed using a dumbbell weight calculated to be 40-50% of the 1RM. Completion
of the exercise protocol was determined to be failure to complete an eccentric
contraction, that is, inability to control the decent of the dumbbell.
Dependant variable
A wireless heart rate monitor (Polar S810i, Polar Electro Oy, Finland) was used to
collect consecutive beat-to-beat electrocardiogram signal, which was later analysed in
HRV Analysis Software v1.1 (The Biomedical Signal Analysis Group, Kuopio,
Finland). The Polar S810i has been validated and good agreement with other
electrocardiogram instruments has been demonstrated.19, 20 All data was stored on a
personal computer for off-line data analysis.
The Short Form McGill Pain Questionnaire (SF-MPQ) was used to measure sensory
and affective qualities of pain and perceived pain intensity.21 A standardised 100mm
horizontal visual analogue scale (VAS) contained in the SF-MPQ, anchored on the
left with no pain and the right with worst possible pain, was also used to measure
pain intensity. The SF-MPQ21, 22 and VAS23, 24 are widely used in research and are
generally considered to be valid and reliable instruments for pain assessment.
63
Procedure
The study was divided into two phases as illustrated in Figure 1. Phase A consisted of
heart rate recording for 15 minutes per day, between the hours of 1600 and 2000, over
five consecutive days. Phase B involved an eccentric exercise protocol on day six
that was intended to induce DOMS, and continued daily heart rate recording and
completion of the SF-MPQ approximately every 12 hours until the end of data
collection on day 14.
HRV
Phase A
10 11 12 13 14
Phase B
TIME
Exercise
Figure 1
Overview of study design.
Phase A comprised of heart rate recording for 15 minutes per day, between the hours of 1600
and 2000, over five consecutive days. Phase B comprised an exercise protocol the morning of
day six, continued daily heart rate recording, and pain intensity reporting every 12 hours.
Each subject received a project information sheet [see Appendix B], operational
instructions for the heart rate monitor [see Appendix C], and a DOMS information
sheet [see Appendix D]. Phase B of the data collection period was outlined to
subjects including the exercise protocol. Correct use of the heart rate monitor was
demonstrated, and subjects practiced placement of equipment and recording of heart
rate in a seated position until deemed by the investigator to be competent and
confident with operation. Each subject was instructed on the daily protocol of data
collection, and requested to refrain from exercise and from consumption of
stimulants, alcohol, and food three hours prior to recording sessions. Subjects were
supplied a nature documentary DVD (The Living Planet)25 to watch during heart rate
recording. Use of the documentary was intended to provide similar recording
conditions between measurement sessions as data collection was undertaken in the
subjects home. The documentary was pre-screened by the investigator and did not
64
contain any content that would potentially startle subjects or evoke strong emotional
responses.
Intervention
Subjects performed the exercise protocol during the morning of day six. Pain
intensity scores were recorded prior to the exercise. The 1RM for the non-dominant
arm was determined, and a dumbbell of approximately 40-50% of the 1RM selected.
Subjects were seated at one end of a standard gym training bench and instructed on
positioning to provide full elbow extension and adequate clearance for the descent of
the dumbbell. Eccentric contraction of the elbow and forearm flexors of the nondominant arm was performed to a count of four seconds. A one second recovery was
included where subjects were assisted in return of the dumbbell to the start position
(fully flexed elbow). Subjects rested for 30 seconds between each set of ten
repetitions and the protocol repeated until subjects failed to complete an eccentric
contraction (i.e. controlled descent of the dumbbell). A summary of the exercise
protocol for each subject is presented in Table 1.
Table 1
Sets performed
S1
20
10
S2
20
10
8.4
S3
20
10
S4
22
12.5
8.4
S5
17
S6
17
Mean
19.3
9.5
6.5
SD
1.9
2.6
1.8
All subjects recorded pain intensity scores immediately after the exercise protocol.
Subjects continued to record heart rate from home in the same manner as Phase A,
with the addition of the SF-MPQ each morning and evening until the end of Phase B.
65
Data Analysis
Data extraction
Beat to beat (R-R) intervals were extracted from the heart rate monitor using
proprietary software (Polar Precision Performance SW, Polar Electro Oy, Finland).
Raw R-R interval data was exported into Microsoft Excel for visual inspection.
Artifact and ectopic beats were replaced with a beat interpolated between the previous
and subsequent normal beats using a method described by the Task Force of the
European Society of Cardiology and the North American Society of Pacing and
Electrophysiology.26 Consistent with established guidelines, data was excluded from
analysis if ectopy was greater than 5% of the recording.26 A clear five-minute period
of heart rate data was extracted from the last two thirds of the 15-minute recording to
minimise movement ectopy. Normalised data was imported into HRV Analysis
Software v1.1 (The Biomedical Signal Analysis Group, Kuopio, Finland). The
software transformed normalised data into statistical time domain measures, a
Poincar plot, and frequency spectra quantified by autoregressive and Fast Fourier
Transform (FFT) (Figure 2). These measures are widely used in research employing
HRV and provide a number of methods to interpret variations in heart rate.26-29
66
S6 D2.txt
Page 1/1
972
RRI (s)
0
1
0.8
0
100
200
300
400
500
Time (s)
600
700
800
900
300
400
500
Time (s)
600
700
800
900
0.1
0
-0.1
0
100
200
Units
Value
(s )
(s )
(1/m in)
(1/m in)
(m s )
(count)
(%)
0.984
0.037
61.07
2.45
26.1
51
5.2
(m s )
0.080
205.0
SD2 = 55.5 m s
(Long-term HRV)
1.15
1.1
SD2
SD1
1.05
RRI
n+1
(s)
1
0.95
0.9
0.85
Distributions*
0.8
0.75
0.8
0.9
1
RRI (s)
1.1
55
0.8
60 65 70 75
HR (beats/min)
0.9
1.1
RRIn (s)
-3
x 10
0.01
PSD (s2/Hz)
PSD (s2/Hz)
0.005
0.1
Frequency
Peak
Band
(Hz)
VLF
0.0391
LF
0.0488
HF
0.2402
LF/HF
0.2
0.3
Frequency (Hz)
Power
(m s 2)
64
394
123
Power
(%)
11.0
67.8
21.2
3.205
0.4
76.2
23.8
4
2
0
0.5
Power
(n.u.)
0.1
Frequency Peak
Band
(Hz)
VLF
0.0000
LF
0.0703
HF
0.2363
LF/HF
*Res ults are calculated from the non-detrended s elected RRI s ignal.
0.2
0.3
Frequency (Hz)
Power
(m s 2)
0
592
115
0.4
Power
(%)
0.0
83.7
16.3
5.141
0.5
Power
(n.u.)
90.4
17.6
Figure 2
Typical Heart Rate Variability Analysis report
Example HRV Analysis report (subject six, day two) illustrating tachogram of normalised R-R interval
data, and transformation of data into statistical time domain measures, a Poincar plot, and parametric
(autoregressive) and non-parametric (Fast Fourier Transform) frequency spectra.
67
For each subject, normalised units (n.u.) of the high frequency (HF) and low
frequency (LF) parameters of HRV were taken from FFT, and plotted with pain
intensity data (VAS units: mm) against time. For the purpose of visual analysis, the
mean of the five baseline data points was calculated for each HRV parameter. The
two standard deviation limits were computed from the mean of the baseline data (days
1-5) and added to each plot of HRV versus time. Trend lines, calculated using simple
linear regression in Microsoft Excel, were also added to Phase A and Phase B of each
graph. Consistent with literature on single-subject designs, visual analysis of changes
in level (i.e. above or below the level of the baseline), trend (upward-sloping,
downward sloping, stationary), and stability of HRV data between phases was
performed.13-15
68
Results
Six healthy males aged 23 to 36 were recruited into the study. Subject characteristics
are presented in Table 2.
Table 2
Subject characteristics
ID
No.
Age
Occupation
36
Height (m)
Weight (kg)
BMI (kg/m )
Routine
physical
activity
1.78
70
22.1
Gym, running
30
1.75
79
25.6
Yoga, cycling
33
Part time
lecturer and land
surveyor
1.66
70
25.4
Squash,
hiking
29
Part time
student and
hospitality
worker
1.83
95
28.4
Gym
23
1.75
75
24.5
Occupation,
tennis
29
1.83
74
22.1
Cycling
All subjects completed the 14 day study. Phase A of data collection consisted of daily
heart rate recording for five consecutive days, between the hours of 1600 and 2000, to
establish baseline HRV. Phase B of data collection consisted of the exercise protocol
on day six which was intended to induce DOMS, continued daily heart rate recording,
and pain intensity reporting every 12 hours until the end of day 14. Four subjects (S1,
S3, S4, and S5) had two days of missing heart rate data. This was due either to
excessive artifact, possibly as a result of electromagnetic interference with the heart
rate monitor equipment, or from human error. For the purpose of analysis, pain
intensity data was subdivided into pre-exercise (day six), immediate post-exercise
(day six), pre-DOMS (days 6-7), DOMS period (days 7-9), and recovery period (days
10-14). The Phase B HRV data was subdivided into pre-DOMS (day 6), DOMS
period (days 7-9), and recovery period (days 10-14).
69
Delayed onset muscle soreness was also apparent in S1, S2, S3, and S4, although
these subjects showed various patterns compared with S6. Subject 4 (S4) reported an
injury to the low back/buttock region and non-dominant arm as a result of a fall
during the evening of day six, and therefore pain intensity scores appear to show no
short-term recovery from the day six exercise protocol. For S2 and S3, the pain
intensity scores show a relatively slow recovery rate from the exercise protocol. In
S2, the immediate post-exercise VAS score reduced by 50% at the end of day six to
70
11mm. This score was followed by peak pain intensity one day later on the morning
of day seven (VAS = 66mm), the peak of DOMS for S2. In S3, the recovery rate
from the exercise protocol was slower, with the immediate post-exercise score
reducing by 23% by the end of day seven to a VAS of 47mm. This score was
followed by peak pain intensity one day later on day eight (VAS = 62mm), the peak
of DOMS for S3.
During the period in which DOMS was expected (days 7, 8, 9), the pain intensity
scores for S5 indicate that the exercise protocol did not induce DOMS in this subject.
The pain intensity scores for S1 during the expected DOMS period only reached 55%
of the immediate post-exercise score of 70mm; however, pain intensity scores indicate
delayed soreness during the expected timeframe of 24-48 hours post-exercise. During
S1s recovery period, pain intensity declined to zero then increased again to 23mm on
day ten. On day ten, S1 reported mild soreness in the hamstring and oblique
abdominal muscles as the result of a routine gym workout on day nine. This increase
in pain intensity was likely due to exercise-induced soreness unrelated to the
experiment. After day ten, pain intensity for S1 gradually declined to zero towards
the end of data collection on day 14 indicating full recovery from muscle soreness
either related or unrelated to the experiment.
In summary, the exercise protocol resulted in reports of pain consistent with DOMS in
S2, S3, S4, and S6, as evidenced by pain intensity scores. The increase in pain
intensity reported by subjects occurred during days 7-9, correlates with literature on
the temporal nature of DOMS (i.e. 24-48 hours after the unaccustomed exercise on
day six).16-18 The exercise protocol resulted in somewhat less satisfactory DOMS in
S1 during days 7-9, and in one subject (S5) DOMS did not occur. As such the high
and low frequency HRV data will only be discussed for S1, S2, S3, S4, and S6.
71
In those subjects in whom DOMS was achieved (S1, S2, S3, S4, S6), no consistent
pattern in the HF data was found that would suggest a relationship between pain
associated with DOMS and HRV. In the subject demonstrating a classic DOMS pain
pattern (S6), the Phase B HF HRV data showed greater fluctuation compared to
baseline and some higher readings, but these readings were not consistently greater
than the baseline mean. In three of the five subjects in whom DOMS was achieved
72
(S3, S4, and S6), the recovery period HF data appeared less stable day to day. In S2,
the HF HRV data throughout Phase B was slightly below the baseline mean and level
compared to an upward-sloping baseline. Data from S2 also showed increased
fluctuation in Phase B data points compared with baseline, but remained stable
overall. In S3, the HF HRV data in Phase B was slightly below the baseline mean,
showed a slight upward-sloping trend line compared to the downward-sloping
baseline, and had greater fluctuation and instability compared to baseline. In
summary, changes to HF HRV data could not be related to pain intensity in the five
subjects in whom DOMS was satisfactorily achieved.
73
S2 - HF & VAS
VAS
HF (n.u.)
S1 - HF & VAS
HF (n.u.)
VAS
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tim e (days)
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time (days)
time (days)
Key:
Phase A
HRV
Baseline
mean
Phase B
HRV
Exercise protocol
day six
2SD
VAS
Figure 3
High Frequency HRV and VAS versus time.
Scatter plot representing five minutes of normalised HF HRV data collected between the hours of 1600
and 2000 over 14 days, with trend lines added to Phase A and Phase B HRV data. Line graph across
days 6-14 representing VAS data collected pre-exercise, immediate post-exercise, end of day six and
every 12 hours from day 7-14. Baseline mean calculated from day 1-5 HF HRV data points. Four
subjects (S1, S2, S4, S5) have one HF HRV data point missing due to human error, and one data point
excluded due to ectopy exceeding 5%.
74
13
14
15
In those subjects in whom DOMS was achieved (S1, S2, S3, S4, S6), no consistent
pattern in the LF data was found that would suggest a relationship between pain
75
associated with DOMS and HRV. In the subject demonstrating a classic DOMS pain
pattern (S6), the Phase B LF HRV data showed greater fluctuation compared to
baseline and some lower readings, but these readings were not consistently lower than
the baseline mean. In three of the five subjects in whom DOMS was achieved (S3,
S4, and S6), the recovery period LF data appeared less stable day to day than the preDOMS period. In S2, the LF HRV data throughout Phase B was slightly above the
baseline mean and level compared to a downward-sloping baseline. Data from S2
also showed increased fluctuation in Phase B data points compared with baseline, but
remained stable overall. In S3, the LF HRV data in Phase B was slightly above the
baseline mean, showed a slight down-slope compared to an upward-sloping baseline,
and had greater fluctuation and instability compared to baseline. In summary,
changes to LF HRV data could not be related to pain intensity in the five subjects in
whom DOMS was satisfactorily achieved.
76
S1 - LF & VAS
VAS
LF (n.u.)
S2 - LF & VAS
LF (n.u.)
VAS
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time (days)
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time (days)
Key:
10
11
12
time (days)
Phase A
HRV
Baseline
mean
Phase B
HRV
Exercise protocol
day six
2SD
VAS
Figure 4
Low Frequency HRV and VAS versus time.
Scatter plot representing five minutes of normalised LF HRV data collected between the hours of 1600
and 2000 over 14 days, with trend lines are added to Phase A and Phase B HRV data. Line graph
across days 6-14 representing VAS data collected pre-exercise, post-exercise, end of day six and every
12 hours from day 7-14. Baseline mean calculated from day 1-5 LF HRV data points. Four subjects
(S1, S2, S4, S5) have one LF HRV data point missing due to human error, and one data point excluded
due to ectopy exceeding 5%.
77
13
14
15
To summarise, the exercise protocol produced muscle failure in all six subjects, that
is, inability to perform one complete eccentric contraction. The exercise protocol also
increased the level of pain in all subjects, as evidenced by immediate post-exercise
pain intensity scores. Pain intensity scores for all subjects, except S4, declined by the
end of day six, although the rate of recovery varied between subjects. During the
expected DOMS period (day 7-9), the level of greatest pain intensity was variable
between subjects. During the recovery period (days 10-14), the DOMS recovery rate
was also variable as S1, S3 and S4 did not have a steady decline in pain intensity,
such as that seen in S2 and S6.
Using visual analysis, there was no correlation between the Phase B pain intensity
scores and changes to the normalised low and high frequency HRV parameters in the
six subjects tested. Although slight differences were observed in the stability of HRV
data and slope and level of trend line with some subjects, no consistent pattern of HF
or LF variation emerged that can be clearly attributed to DOMS. In conclusion, any
effect from DOMS on HRV was not visually identifiable from the results obtained at
the timeframes measured.
78
Discussion
The aim of this study was to determine whether the physiological effects of delayed
onset muscle soreness (DOMS), as a model of mild to moderate musculoskeletal pain,
would influence the autonomic nervous system (ANS) as measured by heart rate
variability (HRV). Heart rate data from six subjects was collected from baseline
through to the pre-DOMS period and from the DOMS period through to full recovery.
Pain intensity data was collected pre-exercise and immediate post-exercise, then
throughout the pre-DOMS, DOMS, and recovery periods. Delayed onset muscle
soreness occurred in 5 out of 6 subjects tested, as evidenced by pain intensity scores,
although visual assessment failed to reveal any consistent pattern between DOMS and
HRV. The results indicate that ANS changes did not occur after induction of DOMS
in the five subjects at the timeframes measured. Although ANS changes were
evident, as indicated by changes to HRV both before and after onset of DOMS, these
changes are more likely attributable to uncontrolled factors such as individual
physiological and environmental variation rather than DOMS.
Outcomes
79
employed DOMS to examine the role of various affective components of pain, such as
fear of pain45 and the role of recalled, expected, and actual pain.46
The pain intensity scores in this study indicate that the exercise protocol was, for the
most part, effective in inducing DOMS, and that DOMS was an effective model of
pain. Completion of the exercise protocol was defined as the inability to perform one
complete eccentric contraction, at which point it was assumed that muscle failure was
achieved. Although the exercise protocol produced muscle failure in all subjects, the
protocol induced a pattern of pain in two subjects which was not a classic DOMS
pattern.17, 47 These two subjects (S1 and S5) appeared to have more upper-body
exercise in their routine physical activities than other subjects: S1 performed pull-ups
as part of a regular gym routine and S5 had a labour intensive occupation (winery
cellar-hand). Muscle failure was achieved in these subjects at the time of the exercise
intervention, yet, they reported less pain during the DOMS period (24-48 hours postexercise) than the immediate post-exercise period. The routine physical activities of
S1 and S5, coupled with the apparent minimal DOMS, suggests that the elbow and
forearm flexor muscles may have been more preconditioned due to the repeated-bout
effect. The repeated-bout effect occurs when subsequent bouts of eccentric exercise,
from 1-10 weeks after the initial bout, produce much less muscle damage implying
an adaptive and protective function.48, 49
80
excluded candidates who were likely to be less susceptible to DOMS of the elbow and
forearm flexor muscles.
In the present study, a pattern that would suggest a correlation between DOMS and
HRV would be a clear shift toward the HF parameter during the DOMS period (24-48
hours post-exercise). A shift towards HF would have indicated increased
parasympathetic activity in subjects during that timeframe.26, 32 By comparison, the
HRV in the same subjects without DOMS, would not display this pattern and only
show normal variation related to respiration and to processes such as circadian
rhythms62 or factors such as posture.63 This comparison is highly simplified however,
as the HRV of healthy subjects is remarkably complex,64 and caution should be
applied when interpreting all HRV data as it is dependent on factors such as age and
gender,65 serum lipoproteins and leukocytes,66 and lifestyle factors67 (for a
comprehensive account see the 1996 Task Force review).26 The results of the current
81
study do not appear to demonstrate a pattern that indicates a shift towards one or other
HRV parameter. Additionally, identification of proportional changes to HF and LF in
the present study was problematic due to difficulty representing five baseline data
points against 14 post-intervention data points.
The low frequency (LF) parameter of HRV represents both sympathetic and
parasympathetic activity to the heart.26 The high frequency (HF) parameter of HRV
represents parasympathetic activity mediated by the vagus nerve.26 As vagal activity
governs respiration, HF is also described as the respiratory frequency. The term
respiratory sinus arrhythmia (RSA) describes spontaneous fluctuations in heart rate
from respiratory-driven vagal modulation of sinoatrial node activity. These
fluctuations result from central coupling between respiratory oscillators in the
brainstem and autonomic outflow.31, 60, 68 Heart rate variability is largely dominated
by ANS activity, however, HRV is an indirect measure of mean autonomic tone.26
For example, HRV data reflects the state and function of the sinoatrial node, humoral
factors, and central heart rate oscillators such as the respiratory centre of the
brainstem.26 Autonomic activity, therefore, is not the sole influence on data obtained
from HRV. A more direct, yet invasive measure, such as microneurography, would
provide a more accurate representation of ANS activity on heart rate but was not
practical for this preliminary study.
Though HRV is an indirect measure of autonomic activity, any potential effect from
DOMS on the ANS may have been of insufficient magnitude to affect HRV. For
example, any change to local physiology from DOMS may have potentially caused
changes in local autonomic fibres, however these changes may have not been potent
enough to potentiate changes in autonomic fibres beyond the perturbed area. In this
type of scenario, any DOMS-induced ANS change would have negligible effect on
HRV.
82
Related research
Although there are no previous studies investigating the effect of DOMS on ANS
indices, there is related research that indicates a possible relationship between the
ANS and injured muscular or articular structures in humans. For instance, Grimm,
Cunningham, and Burke7 published a case series comparing ANS indices in acute
injured subjects and healthy controls. Grimm et al.7 concluded that skin conductance
was statistically greater in the musculoskeletal injury group than in the control group
and that analysis showed a highly significant positive relationship between skin
conductance and SBPLF [systolic blood pressure low frequency]. The greater skin
conductance and higher SBPLF in the acute injured group signifies increased activity
of cutaneous sympathetic neurons and increased activity of vasomotor sympathetic
neurons respectively. Grimm7 surmised that an interaction exists between cutaneous
and vasomotor sympathetic neurons in those with acute musculoskeletal injury, and
that this interaction manifested as altered cardiac and peripheral autonomic function.
Yet, Grimm7 found no difference in the low and high frequency variables between the
injured group and controls, despite the presence of smaller standard deviations in the
injury group.
Various limitations within the investigation by Grimm et al.7 highlight the need for
caution when interpreting their results. To illustrate, heterogeneity from age and sexmatched controls imparts a considerable amount of individual variation when
comparing ANS indices in the two groups. In addition, heterogeneity in the injured
group (e.g. site, duration, and intensity of injury), may have potentially introduced a
number of variables. These include psychological variables associated with low back
pain,69-71 physiological variables associated with density of pain sensitive free-nerve
endings in different tissues (e.g. the meniscotibial ligament of the knee versus the
medial collateral ligament of the knee),72, 73 or variables attributed to central
sensitisation mechanisms associated with injuries of longer duration (e.g. 24 hours
versus six days).74 In addition, it is possible that the routine chiropractic physical
examination given to the injured group and not the control group, biased Grimms7
results. For example, the spinal and cutaneous stimulation during the examination
may have influenced the ANS prior to data collection, although it is difficult to
83
predict how the stimulation would have manifested and how long such influence may
have persisted.
In the present study, the results do not clearly indicate that DOMS produced an effect
on the ANS via HRV. As autonomic activity and pain are highly complex and
individual, there may be a number of influences, both physiological and cognitive,
that may have been a factor in this study. The following section discusses these
influences.
84
than muscle, and was currently believed by researchers to confer a protective effect
due to muscle adaptation.
Inducing DOMS in the non-dominant arm, which is used less frequently in activities
of daily living, may have likewise reduced threat. By comparison, the investigation
by George, Dover, and Fillingim45 induced DOMS in the shoulder muscles of the
dominant arm, which may have been sufficiently threatening to subjects to generate
pain-related fear. This fear had a greater influence on pain perception and fear of
movement, than factors such as anxiety, gender, and catastrophising. Comparing the
present study to the Grimm et al.7 investigation, DOMS was a relatively homogeneous
tissue damage, which could have lessened threat value to subjects. Grimms data may
have been influenced by greater threat, as subjects had naturally occurring injuries
possibly involving heterogeneous tissue damage (e.g. knee injury, shoulder injury),
which may have also been acquired under more threatening circumstances.
Another cognitive aspect to consider in the present study is that previous experiences
of pain can affect the relationship between expected and actual pain responses.82
Dannecker, Price and Robinson46 have reported similar findings to several other
investigations83-86 in that the expectation of pain intensity and unpleasantness
correlated strongly with subsequent pain reports. Investigators are still elucidating the
relative influence of expectation and actual pain on recalled pain; however, it is
conceivable that in the present study, the recall of previous DOMS experiences may
have influenced the expectation of DOMS intensity, and thus pain report. The
influence of recalled, expected, and actual pain may have also played a role in the
Grimm et al.7 investigation, as a naturally acquired injury may have been more
painful, and possibly more threatening, with little or no previous experience of the
tissue damage (e.g. knee injury in a previously untraumatised knee).
Threat is strongly linked with context.40, 75, 87 The experimental environment of the
present study (gym and home) was familiar to subjects, and thus likely interpreted as
being safe. This contrasts with the unfamiliar private and thermo-controlled
autonomic laboratory of the Grimm et al.7 investigation, which may have influenced
ANS indices (e.g. greater skin conductance) more than the present study. The
experimental environment of the present study also included stimuli from a nature
85
Aside from cognitive influences, normal physiological processes could have played a
greater role in the current study. Given that HRV is an indirect measure of the ANS,
the effect on HRV from processes such as circadian rhythms59, 62 and normal
hormonal fluctuation105 may have been of greater magnitude than an effect, if any,
from DOMS. To illustrate, baseline HRV data was very similar in some subjects to
the pre-DOMS and DOMS period data, indicating little overall fluctuation in HRV
from DOMS, even though small differences on certain days may have been evident.
Increased data point density, such as 10 minute Holter recordings taken hourly for 72
hours during the expected DOMS period, may have provided a more accurate
86
The normal physiological response to the exercise protocol performed on day six may
have also played a role. Pober, Braun and Freedson106 have found that even a single
bout of exercise produced changes in HRV similar to that seen in studies on long-term
training. The authors suggest that the changes in autonomic function observed with a
single bout of exercise indicate a shift towards a more stable autonomic environment
for the heart. In the present study, this effect may have potentially been relevant to
the data, as HRV would shift toward HF after the exercise protocol with such an
effect. Unfortunately, however, it is uncertain how long any proposed effects on
HRV from a single bout of exercise might have persisted (e.g. immediate postexercise through to DOMS). Increased density of data points from the post-exercise
period through the DOMS period may have shown more clearly whether this effect
was relevant.
If the physiological changes associated with DOMS do have local or wider effects on
the ANS, the age and good health of the subjects may have compensated for any
potential changes. For example, it is reasonable to infer that the proposed
mechanisms underlying DOMS (micro-damage to muscle tissue and subsequent
inflammation) may have been less challenging to the physiology of a young healthy
subject than tissue damage that was more severe or heterogeneous. To illustrate, the
HRV of a young healthy person is likely more capable of compensating for any
physiological challenge than that of an older person, or one with limited
cardiovascular adaptability.107, 108 Such compensation may have been evident in one
subject of the present study (S4), who sustained a naturally-acquired injury during the
end of day six, the pre-DOMS period. No difference in the pre-DOMS and DOMS
period HRV was observed in this subject, possibly demonstrating the greater
compensation capacity present in a healthy young person.
87
The ECG equipment (heart rate monitor) used in this study has shown good
reliability20 and validity.19 In contrast, the stability of short-term (5-15 minutes) HRV
recordings has shown highly variable reliability coefficients in several
investigations109-111 (for review see Sandercock et al.110), and the poor reliability of
HRV found in previous investigations may be a factor in this study. Another
limitation was that the recording environment of the present study was under limited
control, therefore influences on HRV from factors such as posture and head-tilt may
have been present during recording sessions.110, 112 Similarly, the field setting of the
study limited the ability to inspect and monitor ECG signal quality, or subjects
operation of the heart rate monitor. These factors may have contributed to the ectopy
experienced, despite attempts to control for similarity of recording conditions, time of
recording, and extrinsic influences such as stimulant consumption.
Pain intensity scores during baseline were not collected from subjects: subjects were
pain-free at recruitment and were assumed to remain pain-free throughout the baseline
period. This data may have been useful to compare baseline pain intensity with
baseline HRV. Nonetheless, repeated administration of a pain-related questionnaire
to pain-free subjects during the baseline period could conceivably have lead to
heightened somatic focus, and to higher retest scores. The term somatic focus
describes the tendency to attend to and report somatic symptoms, that is, physical
88
sensations, which do not correlate with objective measures of health status.113, 114
Correlations have been found between increased somatic focus and pain report in a
variety of populations, which potentially could include subjects of the current study.
These populations include younger age groups, those with history of abuse and
affective disorders, and those of lower socioeconomic status.115-118
Use of inferential statistical analysis may have been a beneficial adjunct in terms of
increased sensitivity towards interpreting any potential effect DOMS may have had
on HRV. However, like many single-subject designs, it is probable that the present
study failed to meet parametric assumptions (e.g. normality, equal variance, and serial
independence). Kazdin14 states that statistical analysis may be of value in singlesubject research when there is no stable baseline, the effects cannot be well predicted,
and statistical control may be required for extraneous factors in naturalistic
environments features which are evident in the current study. A number of authors
echo Kazdins sentiment, and spirited debate has occurred between proponents of
both visual and statistical analyses regarding sensitivity and what constitutes a
meaningful change, and in particular the phenomenon of autocorrelation.119, 120, 124-126
Autocorrelation is a statistical term referring to the correlation of a time series with its
own past and future values.119, 123 Such correlation complicates use of inferential
statistical analysis as it violates both parametric and non-parametric assumptions.
Statistical methods that do not account for any trend-related autocorrelation lowers
reliability by distorting effect size magnitude, confidence intervals, and p-values,
regardless of study design.119, 123, 124
89
90
Conclusion
The results of this study indicate that changes to HRV did not occur as result of pain
associated with DOMS within the measurement timeframe employed. Although
slight differences in the stability of HRV data and slope of trend line occurred in some
subjects, no consistent pattern emerged that was attributable to DOMS. If DOMS was
able to influence the ANS, the effect on HRV appeared negligible. Furthermore,
changes to HRV parameters that were evident, were likely attributable to various
physiological and cognitive factors that are known to influence pain perception and
autonomic indices.
To date, the relationship between pain and the ANS has not been fully established: for
example, noxious stimuli clearly and consistently modulates autonomic activity3-5, 10
yet the autonomic effects from mild to moderate pain are less consistent.8, 10
Construction of this study was motivated by a tenet presented within many
osteopathic texts, namely, that musculoskeletal or visceral disturbance can have
effects elsewhere in the body via the ANS.1, 2, 127, 128 Scientific studies to date do not
support this osteopathic concept, and there is a scant amount of literature addressing
this issue.7 The results of the current study, whilst preliminary, did not provide
supportive evidence for this concept, and indeed may even challenge it. There have
been calls in the literature7 for a definitive illustration of whether musculoskeletal or
visceral disturbance could have a deleterious impact on the ANS, and potentially on
health and wellbeing. Establishing the nature and significance of these purported
links is important for evaluating tenets within osteopathy, and may be of clinical
relevance to those with acute injury, or those in chronic pain states.
91
Acknowledgments
Thanks are extended to Mr Darren Lyne for providing the nature documentary DVDs
used in this project.
92
References
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Belova NY, Mihaylov SV, Piryova BG. Wavelet transform: A better approach
for the evaluation of instantaneous changes in heart rate variability. Auton
Neurosci 2007; 131: 107-22.
Radespiel-Troger M, Rauh R, Mahlke C, Gottschalk T, Muck-Weymann M.
Agreement of two different methods for measurement of heart rate variability.
Clin Auton Res 2003; 13: 99-102.
Guzzetti S, Borroni E, Garbelli PE, Ceriani E, Della Bella P, Montano N,
Cogliati C, Somers VK, Malliani A, Porta A. Symbolic dynamics of heart rate
variability: a probe to investigate cardiac autonomic modulation. Circulation
2005; 112: 465-70.
Montano N, Ruscone TG, Porta A, Lombardi F, Pagani M, Malliani A. Power
spectrum analysis of heart rate variability to assess the changes in
sympathovagal balance during graded orthostatic tilt. Circulation 1994; 90:
1826-31.
Terkelsen AJ, Andersen OK, Molgaard H, Hansen J, Jensen TS. Mental stress
inhibits pain perception and heart rate variability but not a nociceptive
withdrawal reflex. Acta Physiol Scand 2004; 180: 405-14.
Molgaard H, Sorensen KE, Bjerregaard P. Circadian variation and influence of
risk factors on heart rate variability in healthy subjects. Am J Cardiol 1991;
68: 777-84.
Scheer FA, Van Doornen LJ, Buijs RM. Light and diurnal cycle affect
autonomic cardiac balance in human; possible role for the biological clock.
Auton Neurosci 2004; 110: 44-8.
Yasuma F, Hayano J. Respiratory sinus arrhythmia: why does the heartbeat
synchronize with respiratory rhythm? Chest 2004; 125: 683-90.
Jensen-Urstad K, Storck N, Bouvier F, Ericson M, Lindblad LE, JensenUrstad M. Heart rate variability in healthy subjects is related to age and
gender. Acta Physiol Scand 1997; 160: 235-41.
Bonnemeier H, Richardt G, Potratz J, Wiegand UK, Brandes A, Kluge N,
Katus HA. Circadian profile of cardiac autonomic nervous modulation in
healthy subjects: differing effects of aging and gender on heart rate variability.
J Cardiovasc Electrophysiol 2003; 14: 791-9.
Yamanaka Y, Honma K. Cardiovascular autonomic nervous response to
postural change in 610 healthy Japanese subjects in relation to age. Auton
Neurosci 2006; 124: 125-31.
Goldberger AL. Non-linear dynamics for clinicians: chaos theory, fractals, and
complexity at the bedside. Lancet 1996; 347: 1312-4.
Agelink MW, Malessa R, Baumann B, Majewski T, Akila F, Zeit T, Ziegler
D. Standardized tests of heart rate variability: normal ranges obtained from
309 healthy humans, and effects of age, gender, and heart rate. Clin Auton Res
2001; 11: 99-108.
Jensen-Urstad M, Jensen-Urstad K, Ericson M, Johansson J. Heart rate
variability is related to leucocyte count in men and to blood lipoproteins in
women in a healthy population of 35-year-old subjects. J Intern Med 1998;
243: 33-40.
Thayer JF, Hall M, Sollers JJ, 3rd, Fischer JE. Alcohol use, urinary cortisol,
and heart rate variability in apparently healthy men: evidence for impaired
inhibitory control of the HPA axis in heavy drinkers. Int J Psychophysiol
2006; 59: 244-50.
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the answer? Behav Ther 2006; 37: 326-38.
Parker RI, Hagan-Burke S. Useful effect size interpretations for single case
research. Behav Ther 2007; 38: 95-105.
Nourbakhsh MR, Ottenbacher KJ. The statistical analysis of single-subject
data: a comparative examination. Phys Ther 1994; 74: 768-76.
Matyas TA, Greenwood KM. Visual analysis of single-case time series:
effects of variability, serial dependence, and magnitude of intervention effects.
J Appl Behav Anal 1990; 23: 341-51.
Kuchera ML, Kuchera WA. Osteopathic principles in practice: 2nd Edition.
Columbus: Greyden Press, 1993. p. 7-12.
Parsons J, Marcer N. Osteopathy: models for diagnosis, treatment and
practice. London: Churchill Livingstone, 2006. p. 107-35.
100
CONSENT FORM
..........(date)
This study has been approved by the Unitec Research Ethics Committee from 26 July 2006 to 31 December 2007. If you have any
complaints or reservations about the ethical conduct of this research, you may contact the Committee through the Chairperson (ph: 09
815-4321 ext 8384). Any issues you raise will be treated in confidence and investigated fully, and you will be informed of the outcome
101
INFORMATION SHEET
Removal of your shirt and placement of a chest strap and wristwatch (this will be loaned to
you to record heart rate). The use of the watch will be fully demonstrated to you. In the
experiment you will set these up for yourself. The researchers will be available by phone to
assist you with setting these up if you experience any technical problems.
Demonstrate that you can confidently operate the watch and correctly locate the chest strap.
Setting aside a consistent time in the same venue (e.g. home) for 14 consecutive days, for 15
minutes each day at a time specified. During this time you will need to wear the heart rate
monitor and transmitter chest strap, while watching a nature documentary that will be
provided to you on DVD or videotape.
Being available to attend Unitec for 30 minutes to perform an exercise protocol on Day 6 of
data collection that will induce muscle soreness (see attached Information Sheet).
Consent to the research teams use of research data in preparing both a research project
dissertation and an article for publication (all data will be anonymised)
Your involvement in this research will aid the understanding of the human bodys response to
eccentric exercise.
The Researchers
The primary researcher is Larissa Morgan
This project is being supervised by Robert Moran and Dr Craig Hilton
102
You have the right to not participate. If you consent but later wish to withdraw from this
research, you may do so at any time up until the point of data analysis (1 week after the last day
of scheduled data collection). This can be done by phoning us, or by telling us when we contact
you that you do not want to participate.
Getting help
Please contact either one of us should you require help with anything regarding this research project.
Larissa Morgan E-mail morgal02@studentmail.unitec.ac.nz
Ph
Robert Moran
()
E-mail rmoran@unitec.ac.nz
Ph
(09) 815 4321 x8642
If you have concerns about the way in which the research is being conducted you can contact the
following:
Health Advocates: Advocates Network Services Trust, Phone (09) 623 5799, 0800 205 555, Fax (09)
623 5798, PO Box 9983, Newmarket, Auckland.
Confidentiality
Confidentiality and your anonymity will be protected in the following ways:
o
Information and data collected from you during the research will be labelled with an
identification number for the sole purpose of anonymously comparing your data between
subsequent sessions.
All computer records will be accessible only by passwords held only by the researchers.
Any data derived from the research will be anonymised and your identity will be kept
confidential.
A copy of the final report will be available at Unitec New Zealand library. All subjects are welcome to
view this. Summaries and recommendations may be published in research journals.
Finally, we would like to thank you for your valuable contribution to this research.
This study has been approved by the UnitecResearch Ethics Committee from 26 July 2006 to 31 December 2007. If you have
any complaints or reservations about the ethical conduct of this research, you may contact the Committee through the
Chairperson (ph: 09 815-4321 ext 8384). Any issues you raise will be treated in confidence and investigated fully, and you will
be informed of the outcome
103
104
INFORMATION SHEET
105
106
Commentaries Include articles that do not fit into the above criteria as original research. Includes
commentary and essays especially in regards to history, philosophy, professional, educational, clinical,
ethical, political and legal aspects of osteopathic medicine.
Clinical Practice Authors are encouraged to submit papers in one of the following formats: Case
Report, Case Problem, and Evidence in Practice.
Case Reports usually document the management of one patient, with an emphasis on presentations that
are unusual, rare or where there was an unexpected response to treatment e.g. an unexpected side effect
or adverse reaction. Authors may also wish to present a case series where multiple occurrences of a
similar phenomenon are documented. Preference will be given to reports that are prospective in their
planning and utilise Single System Designs, including objective measures.
The aim of the Case Problem is to provide a more thorough discussion of the differential diagnosis of a
clinical problem. The emphasis is on the clinical reasoning and logic employed in the diagnostic
process.
The purpose of the Evidence in Practice report is to provide an account of the application of the
recognised Evidence Based Medicine process to a real clinical problem. The paper should be written
with reference to each of the following five steps: 1. Developing an answerable clinical question. 2.
The processes employed in searching the literature for evidence. 3. The appraisal of evidence for
usefulness and applicability. 4. Integrating the critical appraisal with existing clinical expertise and
with the patient's unique biology, values, and circumstances. 5. Reflect on the process (steps 1-4),
evaluating effectiveness, and identifying deficiencies.
Presentation of Typescripts
Your article should be typed on A4 paper, double-spaced with margins of at least 3cm. Number all
pages consecutively beginning with the title page.
To facilitate anonymity, the author's names and any reference to their addresses should only appear on
the title page. Please check your typescript carefully before you send it off, both for correct content and
typographic errors. It is not possible to change the content of accepted typescripts during production.
Papers should be set out as follows, with each section beginning on a separate page:
Title page
To facilitate the peer-review process, two title pages are required. The first should carry just the title of
the paper and no information that might identify the author or institution. The second should contain
the following information: title of paper; full name(s) and address(es) of author(s) clearly indicating
who is the corresponding author; you should give a maximum of four degrees/qualifications for each
author and the current relevant appointment only; institutional affiliation; name, address, telephone, fax
and e-mail of the corresponding author; source(s) of support in the form of funding and/or equipment.
Keywords
Include three to ten keywords. These should be indexing terms that may be published with the abstract
with the aim of increasing the likely accessibility of your paper to potential readers searching the
literature. Therefore, ensure keywords are descriptive of the study. Refer to
http://www.nlm.nih.gov/mesh/meshhome.html for the MeSH thesaurus.
Abstract
Both qualitative and quantitative research approaches should be accompanied by a structured abstract.
Commentaries and Essays may continue to use text based abstracts of no more than 150 words. All
original articles should include the following headings in the abstract as appropriate: Background,
Objective, Design, Setting, Methods, Subjects, Results, and Conclusions. As an absolute minimum:
Objectives, Methods, Results, and Conclusions must be provided for all original articles. Abstracts for
reviews of the literature (in particular systematic reviews and meta-analysis) should include the
following headings as appropriate: Objectives, Data Sources, Study Selection, Data Extraction, Data
Synthesis, Conclusions. Abstracts for Case Studies should include the following headings as
appropriate: Background, Objectives, Clinical Features, Intervention and Outcomes, Conclusions.
107
Text
The text of observational and experimental articles is usually, but not necessarily, divided into sections
with the headings; introduction, methods, results, results and discussion. In longer articles, headings
should be used only to enhance the readability. Three categories of headings should be used:
major ones should be typed in capital letter in the centre of the page and underlined
secondary ones should be typed in lower case (with an initial capital letter) in the left hand margin and
underlined
minor ones typed in lower case and italicised
Do not use 'he', 'his' etc. here the sex of the person is unknown; say 'the patient' etc. Avoid inelegant
alternatives such as 'he/she'. Avoid sexist language.
Statement of Competing Interests
When submitting a Research report you will need to consider if you, or any of your co-authors, are an
Editor or Editorial Board member of the International Journal of Osteopathic Medicine. If this is the
case you will need to include a section, at the end of your manuscript immediately before the reference
section, called "Statement of Competing Interests". Example statement, which may require editing, is
as follows: {Name of author} is an Editor of the Int J Osteopath Med; {Name of author} is a member
of the Editorial Board of the Int J Osteopath Med but was not involved in review or editorial decisions
regarding this manuscript.
References
Responsibility for the accuracy of bibliographic citations lies entirely with the Authors.
Citations in the text: Please ensure that every reference cited in the text is also present in the reference
list (and vice versa). Avoid using references in the abstract. Unpublished results and personal
communications are not recommended in the reference list, but may be mentioned in the text. If these
references are included in the reference list they should follow the standard reference style of the
journal and should include a substitution of the publication date with either "Unpublished results" or
"Personal communication" Citation of a reference as "in press" implies that the item has been accepted
for publication.
Text: Indicate references by superscript numbers in the text. The actual Authors can be referred to, but
the reference number(s) must always be given.
List: Number the references in the list in the order in which they appear in the text.
Examples:
Reference to a journal publication:
1. Van der Geer J, Hanraads JAJ, Lupton RA. The art of writing a scientific article. J Sci Commun
2000;163:51-9.
Reference to a book:
2. Strunk Jr W, White EB. The elements of style. 3rd ed. New York: Macmillan; 1979.
Reference to a chapter in an edited book:
3. Mettam GR, Adams LB. How to prepare an electronic version of your article. In: Jones BS, Smith
RZ, editors. Introduction to the electronic age. New York: E-Publishing Inc; 1999, p. 281-304
Note shortened form for last page number. e.g., 51-9, and that for more than 6 Authors the first 6
should be listed followed by "et al." For further details you are referred to "Uniform Requirements for
Manuscripts submitted to Biomedical Journals" (J Am Med Assoc 1997;277:927-934) (see also
http://www.nejm.org/general/text/requirements/1.htm)
108
Citing and listing of Web references. As a minimum, the full URL should be given. Any further
information, if known (Author names, dates, reference to a source publication, etc.), should also be
given. Web references can be listed separately (e.g., after the reference list) under a different heading if
desired, or can be included in the reference list.
Tables, Illustrations and Figures
A detailed guide on electronic artwork is available on our website: http://www.elsevier.com/authors
Preparation of supplementary data. Elsevier now accepts electronic supplementary material (ecomponents) to support and enhance your scientific research. Supplementary files offer the Author
additional possibilities to publish supporting applications, movies, animation sequences, highresolution images, background datasets, sound clips and more. Supplementary files supplied will be
published online alongside the electronic version of your article in Elsevier Web products, including
ScienceDirect: http://www.sciencedirect.com. In order to ensure that your submitted material is
directly usable, please ensure that data is provided in one of our recommended file formats. Authors
should submit the material in electronic format together with the article and supply a concise and
descriptive caption for each file. For more detailed instructions please visit our artwork instruction
pages at http://www.elsevier.com/authors.
Illustrations and tables that have appeared elsewhere must be accompanied by written permission
to reproduce them from the original publishers. This is necessary even if you are an author of the
borrowed material. Borrowed material should be acknowledged in the captions in the exact wording
required by the copyright holder. If not specified, use this style: `Reproduced by kind permission of . . .
(publishers) from . . . (reference).' Identifiable clinical photographs must be accompanied by
written permission from the patient.
The text of original research for a quantitative or qualitative study is typically subdivided into the
following sections:
Introduction
State the purpose of the article. Summarise the rationale for the study or observation. Give only strictly
pertinent references and do not review the subject extensively. Do not include data or conclusions from
the work being reported.
Materials and Methods
Describe your selection of observational or experimental subjects (including controls). Identify the
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been published but are not well known; describe new methods and evaluate limitations.
Indicate whether procedures followed were in accordance with the ethical standards of the institution or
regional committee responsible for ethical standards. Do not use patient names or initials. Take care to
mask the identity of any subjects in illustrative material.
Results
Present results in logical sequence in the text, tables and illustrations. Do not repeat in the text all the
data in the tables or illustrations. Emphasise or summarise only important observations.
Discussion
Emphasise the new and important aspects of the study and the conclusions that follow from them. Do
not repeat in detail data or other material given in the introduction or the results section. Include
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109
Acknowledgments
In the appendix one or more statements should specify (a) contributions that need acknowledging, but
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AB conceived the idea for the study. AB and CD contributed to the design and planning of the
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110
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